Dermatologic Manifestations of Chronic Disease - PowerPoint Presentation

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Dermatologic Manifestations of Chronic Disease

Shelbi Hayes. M.D.Saints DermatologyOctober, 26 2012Slide2

I. Creating a Framework for Evaluating Skin Lesions

II. Application of the framework to the most common manifestations of chronic diseaseSlide3

I have no financial disclosures.Slide4

Creating a Framework

Question #1Is this a primary or secondary lesion?Slide5

Macule Patch

Papule PlaqueSlide6

Pustule Nodule

Pustule Nodule

Vesicle BullaSlide7

PustuleSlide8

VesicleSlide9

BullaSlide10

WhealsSlide11

WhealsSlide12

Morphologic categories

Macular-PatchPapularPapulosquamous (scaly papules)NodularPustularVesicular-bullous

Urticarial

Petechial

Telangiectasia

Burrow

Poikiloderma

Hyperkeratotic/scale

AtrophicSlide13

Secondary Lesions

CrustErosions and ulcersExcoriationsFissuresScarsLichenification

AtrophySlide14

Creating a Framework

Question #2Is there scale?Slide15

Scale or No Scale?

Scale indicates the disease process involves the epidermis. Lack of scale indicated the disease process affects the dermis or subcutaneous fat.

Exception: Tinea Incognito, Early Vesiculobullous LesionsSlide16

Creating a Framework

Question #3What is the configuration?Slide17

Configuration

AnnularArcuateGeographicDiscreteConfluentSerpiginous

Linear

ReticulatedSlide18

Creating a Framework

Question #4What is the color?Slide19

Color

PinkVioletOrangeBlueGreen

Yellow

Black

BrownSlide20

ColorSlide21

Color

Pink—Pityriasis roseaViolet—Lichen planusOrange—Juvenile xanthogranulomaBlue—Amiodarone skin pigmentation

Green—Pseudomonas

Yellow—Xanthomas

Black—Eschar

Brown—Café au lait spotsSlide22

Creating a Framework

Question #5What is the distribution?Slide23

Immunosuppression Slide24

Herpes SimplexSlide25

Herpes Simplex

Caused by HSV-1 and HSV-2Infections occurs at the primary site, transported via neurons to dorsal root ganglion where latency is establishedPain, tenderness or tingling occur often before reactivation.Grouped vesicles on erythematous base,

however you may not see the primary lesion when the patient presents

!!Slide26
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Herpes Simplex VirusEczema HerpeticumSlide30

Herpes Simplex Virus

Eczema HerpeticumSlide31

Herpes ZosterSlide32

EM-SJS-TEN

Spectrum of epidermal damage +/- mucosal involvementEM minor = no mucous membraneEM in kids usually secondary to HSV, drugs in adultsSJS-TEN constitute one of the few derm emergencies

Treat in burn unit, frozen section of bx to check for necrosis, little inflammation

Fluids, infection prophylaxis, consult ophtho and uro as indicatedSlide33

Erythema MultiformeSlide34
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Erythema Multiforme Major

Also thought to be a hypersensitivity reactionAs with EM minor, but with involvement of ≥2 mucosal surfaces (precedes rash by 1-2 days)

Pronounced constitutional symptoms commonSlide36

Stevens-Johnson Syndrome

Is SJS separate entity from EM major?Some feel SJS is a distinct entity as the rash is more erythematous and less acral than EM majorEM major is more commonly triggered by infections and SJS by drugs.Slide37

Stevens-Johnson SyndromeSlide38

Stevens-Johnson SyndromeSlide39

Stevens-Johnson SyndromeSlide40

Toxic Epidermal Necrolysis

Nikolski’s Sign

= separation of the epidermis from the dermis by rubbing skin between the lesionsSlide41

Toxic Epidermal Necrolysis (TEN)

A life-threatening, exfoliating disease of the skin and mucous membranesHallmark is full-thickness necrosis of the epidermis with separation at the dermoepidermal junction.Slide42

SJS vs TEN

Some use %BSA to define with: <10% = SJS >30% = TENHistologically SJS has a much higher density cell infiltrate (T-lymphocytes) vs TEN (low density macrophages and dendrocytes)Slide43

TEN - Pathogenesis

Majority of cases are likely adverse drug reactions (foreign antigen response).Mean time from drug to onset = 13.6 days Higher risk drugsNSAIDS [38%]Antibiotics [36%] (sulfonamides)

Anticonvulsants [24%] (phenobarb, lamotrigene)

Corticosteroids [14%]Slide44

Use T

rimethoprim-Sulfamethoxazole Judiciously. Up to 17% of patients can have an adverse

cutaneous

reaction.

Occurs within the first 3 weeks.

Warn Patients to alert you immediately.

Do not prescribe if the patient has a family history of sulfa allergy

.Slide45

TEN - Clinical Features

Initial symptoms (1-3 days)Fever (100%)Conjuctivitis (32%)Pharyngitis (25%)Pruritis (28%)Headache, myalgias, arthralgias, vomiting, and diarrhea may occurSlide46

TEN - Clinical Features: Mucosal Involvement

Erosive mucosal lesions (1-3 days before skin eruption) occur in 97%Oral (93%)Ocular (78%)Genital (63%)AnalSlide47

TEN - Clinical Features:Skin Eruption

Burning / painful skin rashUsually begins on face / upper trunkBegins as one of:Diffuse erythema

Irregular bullae

Poorly defined dusky or erythematous macules

Scalp usually sparedSlide48

Multisystem Involvement

GI - Mucosal sloughing in esophagus (dysphagia, GI bleeding)Resp - Tracheal/bronchial erosions

(Respiratory decompensation)

Renal – Glomerulonephritis

Profound fluid and electrolyte disturbancesSlide49

Dermatophytes

Named for area involved: tinea capitis, corporis, manum, facei, pedis, cruris, etc.If there is scale, do KOH exam.

Words of a famous dermatologist:

“If it is scaly, SCRAPE it!”Slide50
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Tinea PedisSlide52

Tinea Cruris-Don’t use steroids!Slide53

Tinea IncognitoSlide54
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ScabiesSlide56

Scabies

Caused by Sarcoptes scabieiPregnant female mite burrows in the stratum corneum, lays eggs about 2-3 per day. Eggs hatch after about a week.See burrows, papules, vesicles.In immunocompromised and elderly, can be crusted and hyperkeratotic (Norwegian also called Crusted Scabies).Slide57

Scabies

Scabies love babies!Scabies love warm, occluded places: axilla, webspaces, groin, head of penisSlide58

Distribution

Pruritic, erythematous papules on the head of the penis=scabies

until proven otherwise.Slide59

Scabies burrowSlide60

Crusted ScabiesSlide61

Verruca Vulgaris

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Verruca Vulgaris

Liquid NitrogenCandida AntigenIL BleomycinCurretage and

cauterySlide63

CondylomaSlide64

Treatment for CA

Avoid liquid nitrogenApply Podophyllin in the office and Rx imiquimod at home.

S, Pniewski T, Malejczyk M, Jablonska S.

Imiquimod is highly effective for extensive, hyperproliferative condyloma in children.

Pediatr Dermatol. 2003 Sep-Oct;20(5):440-2.

Sharquie KE, Al-Waiz MM, Al-Nuaimy AA.

Condylomata acuminata in infants and young children. Topical podophyllin an effective therapy.Slide65

Notify CPS?

CPS should be notified of concerns of possible sexual abuse when ano-genital warts are diagnosed in any child older than 3 years. It also is important for CPS to be educated by the reporting medical provider of other possible nonsexual modes of transmission for the ano-genital warts. Hornor G.

Ano-genital warts in children: Sexual abuse or not?

J Pediatr Health Care. 2004 Jul-Aug;18(4):165-70

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Notify CPS?

For children younger than 3 years, CPS should be notified if other risk factors are noted during assessment, such as an abnormal genital examination, the presence of another sexually transmitted disease, or psychosocial information that warrants investigationHornor G.Ano-genital warts in children: Sexual abuse or not? J Pediatr Health Care. 2004 Jul-Aug;18(4):165-70.Slide67

Recommendations

Child 2 years or younger No report to child protective services needed unless one of the following is present: Abnormality noted on

ano

-genital examination that is of concern for sexual abuse

Another sexually transmitted disease

Psychosocial/behavioral issue that is of concern for sexual abuse

Parental concern of sexual abuse that warrants investigation

Child 3 years or older

Report concerns of possible sexual abuse to child protective services

Nonleading

interview of child regarding sexual abuse concerns (should be completed by a trained forensic interviewer)

Hornor

G.

Ano

-genital warts in children: Sexual abuse or not?

J

Pediatr

Health Care. 2004 Jul-Aug;18(4):165-70. Review. Slide68

Molluscum

ContagiosumSlide69

Molluscum Contagiosum

Caused by pox virusCharacteristic umbillicated papules, molluscum bodies on biopsyMay be an STD in adults – suprapubic and genital lesionsGiant molluscum in AIDS pts, ddx in this pop. includes crypto and other fungal infections

Tx includes cryo, curettage, cantharidin, imiquimod or nothing – they will spontaneously resolveSlide70

Auto-ImmunitySlide71

Lupus

ACLESlide72

Lupus

SCLESlide73

Lupus

DLESlide74

Lupus

Must evaluate all forms of cutaneous lupus for systemic lupusANA, anti-ds DNA, anti-Ro (especially with SCLE), complement levels, UAReview current medications

Treatment is a combination of system steroids and steroid sparing agents (especially

Plaquenil

), mild cases may be treated with only topical steroidsSlide75

DermatomyositisSlide76
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Dermatomyositis

Scalp involvement is relatively common and manifests as an erythematous to violaceous, scaly dermatitis. Clinical distinction from seborrheic dermatitis or psoriasis is occasionally difficult.

Nonscarring alopecia may occur and often follows a flare of systemic disease.Slide79

Dermatomyositis

Heliotrope rash Gottron papulesMalar erythemaPoikiloderma in a photosensitive distribution

Violaceous erythema on the extensor surfaces,

Periungual and cuticular changesSlide80

Dermatomyositis

In 40% of patients, the skin disease may be the sole manifestation at the onset. Muscle disease may occur concurrently, precede, or follow the skin disease by weeks to years.The disease is often intensely pruritic.Systemic manifestations may occur.ROS: arthralgias, arthritis, dyspnea, dysphagia, arrhythmias, and dysphonia.Slide81

Dermatomyositis

Malignancy is possible in any patient with DM, but it is much more common in adults older than 60 years. All adults must be screened.Children with DM may have an insidious onset that hides the true diagnosis until the dermatologic disease is clearly observedSlide82

VasculitisSlide83

Vasculitis

Characterized by size of vessel.Most common cutaneous disease involves small vessels, i.e. leukocytoclastic vasculitis (“Palpable Purpura”).

Medium sized vessel disease includes PAN, Wegeners, and Churg-Strauss.Slide84

Vasculitis

Acronym for DDx of LCV: M

t

S

inai

H

ospital

C

enter

M

eds/

M

alig

S

trep/

S

erum sickness

H

enoch Schonlein/

H

CV

C

onnective tissue disease/

C

ryoglobulinemia

HSP usually <10 y.o. but can be adults, subsequent to URI. IgA around blood vessels Watch renal function.Slide85

Vasculitis Treatment

1. Identify and eliminate underlying cause.

2. If arthralgias present consider starting NSAIDS.

3. Colchicine, dapsone, and immunosuppressive agents may be used if vasculitis is chronic.Slide86
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Fluid OverloadSlide88

Stasis DermatitisSlide89

Stasis DermatitisSlide90

Stasis Dermatitis

Typically affects middle-aged and elderly patients.

Occurs on the lower extremities in patients with chronic venous insufficiency and venous hypertension.

Prevalence is 6-7% in patients older than 50.

This finding makes stasis dermatitis twice as prevalent as psoriasis and only slightly less prevalent than

seborrheic

dermatitis. Slide91

Stasis Dermatitis

Insidious onset of pruritus affecting one or both lower extremities.Reddish-brown skin discoloration is an early sign and may precede the onset of symptoms.The medial ankle is most frequently involved, with symptoms progressing to involve the foot and/or the calf.

H.O. dependent leg edema

H.O. factors that worsen peripheral edema (CHF, HTN with diastolic dysfunction)Slide92

Stasis Dermatitis

Treatment is two-fold:Relief of symptoms Treatment of underlying venous insufficiencyFor pruritus and eczematous component:

Class IV or V topical corticosteroids and emollients (AVOID NEOMYCIN)

Daily use of support stockingsSlide93

Id Reaction

Autosensitzation

dermatitis

Most often pts with stasis and contact dermatitis

Follows primary lesions by days to

weeks

Treatment includes treatment of inciting event, topical and IM steroidSlide94

Pruritus

Extremely common in patients with chronic renal failure Much more common in patients on renal dialysis vs peritoneal dialysisIndependent marker for mortality for patients of

hemodialysisSlide95

Pruritus

Antihistamines of some helpDoxepinTopical capsaicin cream or Sarna lotionEfficient hemodialysisUVBSlide96

DiabetesSlide97

Eruptive Xanthomas

Patients with poorly controlled glucose and elevated triglycerides

Resolution with tight glucose controlSlide98

Necrobiosis Lipoidica

Diabeticorum

0.03% of patients with diabetes

Resolution or progression is not related to glucose control

Very difficult to treat

Topical or IL steroid

Topical

tacrolimus

Surgical excision (often recur)Slide99

Acanthosis Nigricans

Associated with obesity and insulin resistance

Improved with weight loss and glucose control

Treatment includes topical

retinoids

and salicylic acidSlide100

Diabetic Bullae

Appears on background of normal skin

Resolves spontaneously

Culture fluid for secondary infection of it appears cloudySlide101

Diabetic Dermopathy

Patients with poorly controlled diabetes

Correlates with

vacsular

damage secondary to diabetes

No treatment needed

thought to improve with improved glucose controlSlide102

“More is missed by not looking than by not knowing”

M. McKay, M.D.